dc.creatorUniversidad San Sebastián
dc.creatorUniversidad San Sebastián
dc.creatorUniversidad San Sebastián
dc.creatorUniversidad San Sebastián
dc.creatorUniversidad San Sebastián
dc.creatorUniversidad San Sebastián
dc.creatorUniversidad San Sebastián
dc.creatorUniversidad San Sebastián
dc.creatorUniversidad San Sebastián
dc.creatorTorres-Estay, Verónica
dc.creatorMastri, Michalis
dc.creatorRosario, Spencer
dc.creatorFuenzalida, Patricia
dc.creatorEcheverría, Carolina E.
dc.creatorFlores, Emilia
dc.creatorWatts, Anica
dc.creatorCerda-Infante, Javier
dc.creatorMontecinos, Viviana P.
dc.creatorSotomayor, Paula C.
dc.creatorAmigo, Julio
dc.creatorEscudero, Carlos
dc.creatorNualart, Francisco
dc.creatorEbos, John M.L.
dc.creatorSmiraglia, Dominic J.
dc.creatorGodoy, Alejandro S.
dc.date.accessioned2023-05-24T04:54:29Z
dc.date.available2023-05-24T04:54:29Z
dc.date.created2023-05-24T04:54:29Z
dc.date.issued2022-10
dc.identifier2072-6694
dc.identifierhttps://repositorio.uss.cl/handle/uss/6656
dc.identifier10.3390/cancers14194750
dc.description.abstractThe survival of patients with solid tumors, such as prostate cancer (PCa), has been limited and fleeting with anti-angiogenic therapies. It was previously thought that the mechanism by which the vasculature regulates tumor growth was driven by a passive movement of oxygen and nutrients to the tumor tissue. However, previous evidence suggests that endothelial cells have an alternative role in changing the behavior of tumor cells and contributing to cancer progression. Determining the impact of molecular signals/growth factors released by endothelial cells (ECs) on established PCa cell lines in vitro and in vivo could help to explain the mechanism by which ECs regulate tumor growth. Using cell-conditioned media collected from HUVEC (HUVEC-CM), our data show the stimulated proliferation of all the PCa cell lines tested. However, in more aggressive PCa cell lines, HUVEC-CM selectively promoted migration and invasion in vitro and in vivo. Using a PCa-cell-line-derived xenograft model co-injected with HUVEC or preincubated with HUVEC-CM, our results are consistent with the in vitro data, showing enhanced tumor growth, increased tumor microvasculature and promoted metastasis. Gene set enrichment analyses from RNA-Seq gene expression profiles showed that HUVEC-CM induced a differential effect on gene expression when comparing low versus highly aggressive PCa cell lines, demonstrating epigenetic and migratory pathway enrichments in highly aggressive PCa cells. In summary, paracrine stimulation by HUVEC increased PCa cell proliferation and tumor growth and selectively promoted migration and metastatic potential in more aggressive PCa cell lines.
dc.languageeng
dc.relationCancers
dc.titleThe Differential Paracrine Role of the Endothelium in Prostate Cancer Cells
dc.typeArtículo


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